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TIM-3 Inhibition Enhances Tumor Progression and Metastasis: A Paradoxical Immune Checkpoint Response

ABSTRACT: Syngeneic breast tumors were developed by inoculating of 4T1 cells, into the left flank of female Balb/c mice. When tumor volume reached 200-250 mm3, mice were selected randomized way to receive the treatment of anti-TIM-3 monoclonal antibody (mAb) (Clone: RMT3-23, BioXcell, cat. # BE0115, RRID: AB_10949464). Anti-TIM-3 mAb (250 µg/injection) was administered via the intraperitoneal (i.p.) route. Primary tumors were allowed to developed for up-to 40 days. Primary tumor histology, liver metastasis, and serum cytokine and tumor tissue proteome were analysed and compared between the control tumor and TIM-3 antibody treated tumor.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Breast

DISEASE(S): Breast Cancer

SUBMITTER: ANUPAM BASU

LAB HEAD: ANUPAM BASU

PROVIDER: PXD065028 | Pride | 2025-12-29

REPOSITORIES: Pride

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			Action	DRS
	M01_1.msf	Msf
	M01_1.raw	Raw
	M01_2.raw	Raw
	M01_3.raw	Raw
	M02_1.raw	Raw

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Publications

TIM-3 inhibition enhances breast tumor progression and metastasis: A paradoxical immune checkpoint response.

Dolui Barnali B Majumdar Banani B Bandyopadhyay Arghya A Desai Kartiki V KV Basu Anupam A

The Journal of biological chemistry 20251222

T cell immunoglobulin and mucin-domain containing-3 (TIM-3) is an emerging immune checkpoint receptor. Blocking immune checkpoint signals is a promising strategy for cancer immunotherapy. While TIM-3 blockade is currently under clinical investigation, its context-dependent role remains poorly understood. This study investigates the molecular consequences of TIM-3 inhibition using an experimental murine breast tumor model. Contrary to therapeutic expectations, administration of an anti-TIM-3 mono ...[more]

PMID: 41443412

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Tim-4+ Cavity-Resident Macrophages Impair Anti-Tumor CD8+ T cell Immunity [RNA-Seq]

Project description:Here we report RNA sequencing data from sorted Tim-4low vs Tim-4high macrophages in steady-state (no tumor) mice and also MC38-LG-tumor-bearing animals that were treated with isotype or anti-Tim-4 antibody.

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Expression data from murine gut and spleen tissues

Project description:TIM-1 is a gene that regulates immune responses including transplantation tolerence, allergy and asthma, autoimmunity, viral infections as well as cancer, however its role in transplantation has not been evaluated. Here we use a murine model of graft versus host disease (GVHD) to evaluate the therapeutic potential of blocking TIM-1 using an antibody. We used microarray data to look for difference in gene expession in the gut which is one of the main organs that are afffected by GVHD as well as the spleen an organ when the immune response is generated. This will give us evidence as to whether the blocking TIM-1 mAb may modulate the immune response and protects against GVHD and promoted a less proinflammatory immune response

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Histone H1 profiling in breast cancer samples

Project description:Epigenetic aberrations have been recognized as important contributors to cancer onset and development, and increasing evidence suggests that linker histone H1 variants may serve as biomarkers useful for patient stratification, as well as play an important role as drivers in cancer. Although traditionally histone H1 levels have been studied using antibody-based methods and RNA expression, these approaches suffer from limitations. Mass-spectrometry (MS)-based proteomics represents the ideal tool to accurately quantify relative changes in protein abundance within complex samples. We used a label-free quantification approach to simultaneously analyze all somatic histone H1 variants in breast cancer patient samples (different areas laser-microdissected from the same tumor sections, and triple negative samples with/without relapse 3 years after chemotherapy.

2021-03-16 | PXD020524 | Pride

TCR repertoire analysis revealed the mobilization of novel CD8+ T cell clones into Cancer-Immunity Cycle following anti-CD4 antibody administration

Project description:Depletion of CD4+ cells by anti-CD4 monoclonal antibody (anti-CD4 mAb) induces expansion of tumor-reactive CD8+ T cells and exhibits strong antitumor effects in several murine tumor models. However, whether the anti-CD4 mAb treatment activates particular or a broad variety of tumor-reactive CD8+ T cell clones is not answered. To investigate the changes of TCR repertoire induced by the anti-CD4 mAb treatment, we performed unbiased high throughput TCR sequencing in a B16F10 mouse subcutaneous melanoma model.

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Transcription profiling of mouse IgE/antigen-activated mast cells stimulated with TIM-3

Project description:TIM-3 is known to be expressed on dendritic cells, monocytes, melanoma cells, mast cells and on activated Th1 cells. In activated Th1 cells, stimulating TIM-3 by one of its ligands, galectin-9, leads to apoptosis and thus it plays a central role in terminating Th1-type immune responses. Interestingly, in IgE/antigen-activated mast cells TIM-3 enhances the production of IL-13 and IL-4. To get a more complete picture about the gene expression changes induced by TIM-3 in mast cells, in vitro differentiated mouse immature mast cells were stimulated by an agonist anti-TIM-3 antibody and IgE-sensitized mouse immature mast cells were activated by antigen and an agonist anti-TIM-3 antibody for 2 or 16 hours (overnight). Experiment Overall Design: Bone marrow cells were differentiated in RPMI + 10% FCS + 5 ng/ml mouse IL-3 + 40 ng/ml mouse SCF for >4 weeks. The purity of the cell cultures was >90% at this time point (FcERIa+/c-kit+ cells). These in vitro-differentiated immature mast cells were then treated by either control goat IgG or an agonist anti-mouse TIM-3 antibody (RnD Systems, 15 ug/ml for 2 or 16 hours). For the IgE/antigen-activated mouse mast cells, these in vitro-differentiated immature mast cells were sensitized by 5 ug/ml anti-DNP IgE (Sigma) for 1 hour and then treated with 100 ng/ml DNP-HSA (antigen, Sigma) and either control goat IgG or an agonist anti-mouse TIM-3 antibody (RnD Systems, 15 ug/ml) for 2 or 16 hours. The anti-TIM-3 samples were labeled by Cy5 and they were compared to the Cy3-labeled, goat IgG controls in a dual-color, paired experimental setup. The Agilent Whole Mouse Genome 4x44K expression microarray kit and Dual-Color Protocol version 5.5 were used in the experiments.

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Syndecan-1-targeted therapeutic antibody inhibits macropinocytosis and induces antitumor immunity in pancreatic cancer

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Nogo-B co-IP-MS experiment in mouse liver and pancreas

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Single cell TCR-seq profiling of T cells isolated from LNs of MC38 tumor-bearing mice

Project description:We investigate the single-cell landscape of the inflammatory mouse tumor model MC38, a C57BL/6 tumor cell line derived from colon adenocarcinoma. MC38 (diluted in HBSS and matrigel) was inoculated in the right unilateral flank (in the border of positions B2 and B3) of C57BL/6 mice (ref Study 16-3384 AV). Draining lymph nodes were taken one day after group-out (average 150-250 mm3 tumor size at day 0), approximately 14-19 days. Draining lymph nodes were dissociated and flow sorted accordingly to obtain the cells for 10x Chromium 5' Gene Expression Profiling and TCR sequencing.

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The effect of TIM-3 stimulation on the gene expression profile of IgE/antigen-activated mouse mast cells

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